[Lateral peroneal cutaneous nerve entrapment in the leg].
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Biomedical subjects
Publications and source records attributed to B Godes-Medrano.
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AIM: Two patients suffering from congenital insensitivity to pain were studied. They corresponded to types IV and V of the 'hereditary sensory and autonomic neuropathies' (HSAN) classification. CASE REPORTS: The first case showed important autonomic dysfunctions, such as anhidrosis, hyperthermia, skin and bone trophic impairment, and mental retardation; the second one only exhibited alterations in pain and temperature sensibilities. In both, chronic indolent corneal ulcers were also present. Conventional neurophysiological evaluation of the neuromuscular system was normal, but an afferent disturbance of the blink reflex (BR) was evident in both. The sympathetic skin response was absent in the HSAN type IV case and normal in the HSAN type V. Notable reduction of the small myelinated fibres, associated to almost no unmyelinated fibres in the first case, were found in the sural nerve biopsies. CONCLUSIONS: So far there haven't been described BR abnormalities in patients with congenital insensitivity to pain, which should be related to a trigeminal sensory impairment, which could explain the corneal ulcers that suffered these cases. BR studies should be included in the neurophysiological evaluation of the suspected small fibre neuropathies even when there are no facial symptoms shown.
UNLABELLED: OBJECTIVE-PURPOSE: The purpose of this case report is to describe a gait disorder presenting as a bilateral sacral radiculopathy after vigorous cycling. Also, we discuss the pathogenic mechanisms and we revise the bibliography. PATIENT AND METHODS: The patient complained of a rapid painless weakness in legs, after intense and prolonged cycling 4 months ago. The physical and electromyographical examinations revealed important weakness in foot and knee flexors, and signs of acute denervation with mixed reinnervation (active and chronic) in myotomal S1 muscles, respectively. The lumbo-sacral magnetic resonance imaging were normal. The follow-up studies demonstrated gradually improvement in clinical and neurophysiological parameters. DISCUSSION: We established that our patient presented a subacute bilateral S1 radiculopathy and we confirmed the progressive clinical and neurophysiological improvement. The radiculopathy are infrequent in cyclists, and its common origin is the external compressive aggression. In our patient we speculate and discuss that this radicular lesion could present different pathogenic mechanisms: the elongation, the compression and the secondary vasanervorum ischemia. In our knowledge S1 radiculopathy related to compressive lesions in sportsmen has not been previously described.
PURPOSE: We report autosomal dominant distal muscular dystrophy in 5 members of a Spanish family. INTRODUCTION: This unusual muscular disorder has late adult onset and predominantly it affects the anterior compartment of the legs. This myopathy presented clinical and electromyographical characteristics, but unspecific histological findings. Early there have appeared genetical studies, the most frequently used is chromosome linkage, but it is not an absolute criterion for diagnosis, and it is not available in most hospitals. PATIENTS DESCRIPTIONS: In our cases walking difficulties appeared between the fourth and fifth decades, characterized by progressive and varied weakness with amyotrophy in the tibial anterior compartment. The electromyography confirmed the presence of a severe non-inflammatory myopathy, chronic and symmetric in the pretibial muscles and of less intensity in the calf muscles. The levels of creatine phosphokinase were normal and muscle biopsy identified a chronic, unspecific lesion with important fibrosis. CONCLUSIONS: The findings, although with some phenotypical differences, were those commonly found in Markesbery-Griggs disease, tibial muscular dystrophy or late onset type 2 distal myopathy. We report a family affected by this muscular disorder, we describe the differential diagnosis and we discuss the review of the available literature.
INTRODUCTION: Polyneuropathies (PNP) result from damage to a number of nerves. They are classified according to the anatomical-functional, histological, aetiological and genetic characteristics. Here we report on the prolonged follow-up carried out on an adult male who had a chronic recurring axonal-type PNP. CASE REPORT: We describe the case of a 65-year-old male who presented episodes of neurological deficit over a period of 10 years that were interspersed with prolonged, stable periods in which he was free of new symptoms. The patient's functional limitations became greater with each successive relapse and the situation is now one of extreme disability. The characteristics of the clinical picture pointed towards a diffuse peripheral nerve disorder, and the neurophysiological studies carried out revealed polyneuropathic, sensory and motor injury mediated by an axonal mechanism with no associated demyelination. A comprehensive analytical, imaging and functional study was conducted, but did not reveal any specific causes. The particular clinical process, the exclusion of other pathologies and the electrophysiological findings allowed us to reach a diagnosis of recurring or episodic chronic primary axonal PNP. CONCLUSIONS: This description can be added to the few cases reported in the literature. As we see it, this is an unusual, although probably underdiagnosed, disease and it must be taken into account in the differential diagnosis of chronic recurring PNP because of the diagnostic implications and--with respect to its usually poor response to therapy--due to the prognoses.